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FBS2 > Immunity and Infection > Flashcards

Immunity and Infection Flashcards

1
Q

What are the characteristics of the innate immune response?

A

Non-specific; used immediately or within several hours after exposure to antigen (0-4h); responds the same way every time; distinguishes between self and non-self; induces and directs the acquired immune response

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2
Q

What are the components of the innate immune response?

A

Physical/anatomical barriers; secreted compounds (cytokines, antibacterial compounds, complements, natural antibodies); cellular components (phagocytes, NK cells)

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3
Q

When, after exposure to the antigen, does the acquired immunity (adaptive immunity) begin?

A

> 96 hours

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4
Q

How does the skin prevent entry of pathogens?

A

Secretes anti-microbial compounds (against E. Coli)

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5
Q

How do tears, sweat and saliva prevent the entry of pathogens?

A

Contain lysozyme –> destroy bacterial cell wall

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6
Q

How does the innate immune response recognise the pathogen?

A

Recognises PAMPs

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7
Q

How are gram negative and gram positive bacteria differentiated?

A

GRAM NEGATIVE: small peptidoglycan component, presences of outer membrane containing lipopolysaccharide (LPS): lipid A (PAMP part), O polysaccharide (tells you which type of bacteria it is)
GRAM POSITIVE: big peptidoglycan component, no outer membrane, teichoic and lipoteichoic acid present

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8
Q

Which are the pattern recognition receptors (PRR)?

A
  1. Collectins (serum)
  2. Toll-like receptors (membrane)
  3. Nod-like receptors (cytoplasm)
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9
Q

What are collectins and how do they work?

A

Family of proteins present in solution; collagen structure: interacts with effector parts of the immune system; lectin region: binds to sugar molecules on surface of pathogen (mannose)

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10
Q

What are toll-like receptors and how do they work?

A 
Membrane bound receptors:
TLR1: gram+ bacteria
TLR2: gram+ bacteria + mycoplasma
TLR3: RNA virus (dsRNA)
TLR4: gram- bacteria
TLR5: flagellin
TLR6: micoplasma
TLR7: RNA virus (ssRNA)
TLR8: RNA virus (ssRNA)
TLR9: unmethylated CpG DNA
TLR10: ?
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11
Q

What are Nod-like receptors and how do they work?

A

Intracellular PRR; NOD-1 –> gram+ bacteria; NOD-2 –> all bacteria

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12
Q

Which are the effector mechanisms of the innate immune system?

A
  1. Complement
  2. Phagocytosis and killing
  3. Cytokines
  4. Activation of adaptive immunity
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13
Q

How does complement work and for which pathogens is it important?

A

Important for bacteria; operate via cascade activated by 3 pathways (classical, MB-lectin, alternative); induce activation of C3 by C3 convertase:

  1. C4a, C3a, C5a: recruitment phagocytosis
  2. C3b: opsonization
  3. C5b, C6,7,8,9: membrane attack complex –> lysis
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14
Q

What are the key players in phagocytosis?

A

Macrophage: maturates from circulating monocytes, large numbers in GI tract, spleen, liver and lungs, long-lived
Neutrophil: found only in blood unless activated, short-lived

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15
Q

What are the killing mechanisms of macrophages and neutrophils?

A

Neutrophils: reactive oxygen intermediates –> NADPH oxidase on surgace of phagosome forms hydroxil radicals and hypochlorite –> DNA damage and alterations in bacterial membranes
Macrophages: reactive nitrogen intermediates –> cytokines –> inducible NO synthetase –> conversion of O2 and L-arginine to NO and L-citrulline –> DNA damage and alterations in bacterial membranes

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16
Q

What are cytokines?

A

Proteins that act as intercellular messengers, can be activating or deactivating
Innate response: mostly activating (IL1,6, TNF-alpha)
Adaptive: also deactivating

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17
Q

What are chemokines and what are some examples?

A

Class of cytokines with chemoattractant properties; promote inflammation by allowing cells to adhere to the surface of blood vessels and migrate to the infected tissue; pleiotropic; four families;
IL-8: produced by macrophages and endothelial cells –> recruits neutrophils to site of infection

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18
Q

What are interferons and how are they classified?

A

They are a class of cytokines:
Type 1: IFNalpha and beta –> response in virally infected cells –> activate NK cells
Type 2: IFNgamma –> antimicrobial killing, mostly adaptive immune response

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19
Q

What is the function of NK cells?

A

Kill virally infected cells and tumor cells, responsive to TNFalpha, IL-12; produce IFNgamma

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20
Q

What are the functions of IL1,6, IL12, IL8 and TNFalpha?

A

IL-1,6 —> inflammation and fever
IL-12 —> CD4 T cell differentiation
TNF-alpha —> fever, macrophage activation
IL8 —> produced by macrophages and endothelial cells —> recruits neutrophils to site of infection

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21
Q

What are the 3 types of antigen presenting cells?

A

Macrophages, B cells, dendritic cells (usually present as immature round cells displaying PRR; maturation leads to dendrites and expression of MHC and CD molecules

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22
Q

What is the structure of the T cell receptor and where are T cells developed?

A

Heterodimer: alpha and beta chain or gamma delta with variable and constant regions
Developed: thymus

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23
Q

What is the structure of the B cell receptor and where are B cells developed?

A

Two identical heavy chains and two identical light chains; two antigen-binding sites per antibody
Development: bone marrow

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24
Q

What are the timings for the primary and secondary responses in adaptive immunity?

A

Primary: 12 days
Secondary: 5-7 days

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25
Q

What are the variable regions of the heavy and light chains composed of?

A

Heavy chain variable region (chromosome 14): V, D, J

Light chain variable region: V and J only

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26
Q

What is gene rearrangement important for?

A

Combinatorial diversity and junctional diversity (terminal deoxynucleotide (TdT))

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27
Q

What are the two groups of T cells?

A

Cytotoxic T cells (CD8): secrete cytotoxic granules, T cell receptor is not needed after recognition of antigen
Helper T cells (CD4): differentiate to produce different sets of cytokines (Th1, Th2, Th17, Treg)

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28
Q

What does B cell activation lead to?

A

Production of plasma cells –> secretion of antibodies

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29
Q

What is the structure of immunoglobulins?

A

Two heavy chains and two light chains;
Variable region determines specificity (kappa or lambda);
Constant region of heavy chain determines function of antibody (isotype)

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30
Q

Which type of bonds link the heavy and light chains of antibodies?

A

Disulfide bonds

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31
Q

What are the four functions of antibodies?

A
  1. Neutralisation
  2. Opsonisation
  3. Activation of the component cascade
  4. Agglutination of particles
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32
Q

What are the characteristics of IgG?

A

Main one in serum; response to vaccines; 4 subtypes; goes on to placent; opsonisation; activation of NK cells

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33
Q

What are the characteristics of IgA?

A

Serum: monomer
Mucosal surfaces: dimer with joining J chain
Important in the gut; agglutination and neutralisation; crosses placenta and found in breast milk

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34
Q

What are the characteristics of IgM?

A

First antibody made in immune responses; pentameric (10 possible binding sites); agglutination; too big to cross placenta; can activate complement cascade better than IgD

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35
Q

What are the characteristics of IgE?

A

Association with mast cells (mast cell degranulation) –> allergies; parasite infection

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36
Q

What are the characteristics of IgD?

A

Occurs on surfaces of naive B cells; very little in serum

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37
Q

What is affinity maturation?

A

Occurs only for B cells; with the help of T cells, B cells can enter germinal centres in secondary lymphoid tissue after encountering the antigen –> rapid division:

  1. Somatic hypermutation: mutation of immunoglobulin variable region, requires activation induced cytidine deaminase (AID)
  2. Selection: for higher affinity
  3. Possible class switch
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38
Q

Which two types of cells leave the germinal centres?

A

Quiescent circulating memory B cells; affinity maturated possibly class switched

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39
Q

What are chimeric antibodies?

A

Mouse variable region + human constant regions (-ximab)

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40
Q

What are humanised antibodies?

A

Only parts of the variable region that come in contact with the antigen are from the mouse (-zumab)

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41
Q

What type of ending do human monoclonal antibodies have?

A

-umab; adalimumab –> against TNFalpha

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42
Q

What are the differences between MHC I and II

A

MHC I: monomer, associated with beta2 microglobulin, endogenously expressed on all nucleated cells, binds to 8-10 aa, important in viral infections and tumors, endogenous proteins
MHC II: heterodimer (alphabeta), expressed on specialised antigen presenting cells, binds to 10-15 aa, exogenous proteins

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43
Q

Where are the genes coding for MHC I and II situated?

A

Chromosome 6; 3 different HLA coding for MHC I and 3 for MHC II; polygenic and polymorphic

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44
Q

How does T cell activation occur?

A

Signal 1: TCR and MHC complex (CD4 with MHC II and CD8 with MHC I)
Signal 2: co-stimulation (CD80/86 with CD28)
Signal 3: APC secretes cytokines to direct differentiation of CD4 T cells
Activation –> division and production of cytokines

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45
Q

Which types do CD4 T cells differentiate in and which cytokines are produced?

A

Th1: IL2, IFN-gamma, response to intracellular pathogens (TB, listeria, leprosy) and viruses, macrophages and CD8 T cells
Th2: IL4, IL13, responses to extracellular parasites (schistosomes), promote B cell maturity
Th17: IL17,21,22, important in the gut (parasites), extracellular bacteria and fungi, help epithelium and fibroblast, neutrophil chemotaxis
Treg: TGFbeta and IL10, adaptive and innate immune response control

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46
Q

Which cytokines help naive T cell differentiation?

A

IL6,12 and TNFalpha

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47
Q

How does thymic education work?

A
  1. Obtain functional TCR
  2. Positive selection for self MHC (cortex) with specialised APC: select CD4 or CD8
  3. Negative selection to eliminate high affinity self-reactive T cells: thymic medullary epithelial cells (TMECs) express tissue specific antigens (TSAs)
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48
Q

Which are the TSAs represented by the liver, pancreas, islets of langerhans, eye, thyroid?

A 
Live: serum amyloid P
Pancreas: trypsin
Islets of langerhans: insulin
Eye: cristallin
Thyroid: thyroglobulin
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49
Q

Which are the peripheral mechanisms of immune tolerance?

A

Anergy: T cell remains in circulation but is unresponsive to future stimulation (signal 1 but not 2)
Rregulatory T cells: decrease proliferation, cytokine production, reduce co-stimulation, alter cytokine production

50
Q

What are the two types of regulatory T cells?

A

nTreg: produced in thymus, respond to self antigens, important for autoimmunity
aTreg: develop in periphery, constant low level exposure of antigen, regulation for responses to food antigens

51
Q

What is IPEX?

A

Multiple autoimmune diseases developed by individuals lacking nTregs

52
Q

How and where does activation of naive lymphocytes occur?

A

Dendritic cells move to lymph nodes: secrete cytokines and chemokine —> up regulation of adhesion molecules of endothelial venules —> increase in migration of naive T cells into the lymph node

53
Q

Which types of cells play a role in immunological memory?

A

Plasma cells: live for year, high affinity antibodies, protective immunity
B cells: high frequency, can develop into plasma cells
Memory t cells: higher frequency before primary infection, immediate effector function

54
Q

What is inflammation?

A

The reaction of vascularised living tissue to local injury

55
Q

What are the four signs of inflammation?

A

Redness; swelling; heat; pain

56
Q

Which are the vascular changes in acute inflammation?

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilation and increased blood flow
  3. Slow of the circulation because of increased permeability of the microvasculature (stasis)
  4. Exudation of plasma proteins and fluid (oedema)
57
Q

What are the differences between exudates and transudates?

A

Exudates: inflammatory extravascular fluid that has a high protein concentration, much cellular debris and SG above 1020
Transudates: ultrafiltrates of low protein content

58
Q

What is pus?

A

A purulent exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris

59
Q

How does margination occur?

A

Inflammation –> histamine (C5a or LPS) and thrombosis factors –> weibel-palade bodies within endothelium release cell adhesion molecules (P and E selectin) –> neutrophils slow down and roll on the endothelium

60
Q

What happens to neutrophils after margination?

A
  1. Release of IL8 attracts neutrophils along concentration gradient
  2. Chemotaxis in response to: bacterial products, complement components (C5a), products of lipooxygenase pathway of arachidonic acid metabolism (leukotriene B4)
  3. Diapedesis and extravasation: interaction btw integrin molecules on leukocytes and ICAM-1 on endothelium
61
Q

What are the differences between acute suppurative, fibrous and membranous inflammation?

A

Suppurative: presence of puss (accumulation of neutrophils), appendicitis
Fibrous: fibrin + neutrophils (lobal pneumonia)
Membranous: inflammatory membrane forms over inflamed tissue (diphteria, pseudomembranous colitis)

62
Q

What is the histology of chronic inflammation?

A
  1. Infiltration by mononuclear cells: macrophages, lymphocytes and plasma cells
  2. Proliferation of fibroblasts and small blood vessels
63
Q

What are granulomas?

A 
Formed from macrophages due to chemokine release;
Early granuloma (macrophages + lymphocytes):
1. non-caseating epitheloid granuloma (+ fibroblasts producing collagen)
2. caseating epitheloid granuloma (+ fibroblasts producing collagen)
64
Q

What are some examples of granulomas?

A
  1. Foreign body granuloma
  2. Pulmonary tubercolosis: granulomatous inflammation
  3. Paraffin oil
65
Q

What is atopy?

A

Inherited tendency to make immediate hypersensitivity responses due to mast cell degranulation and histamine release (wheal and flare)

66
Q

What are common therapies for immediate hypersensitivities/allergies?

A

anti-histamines, beta2-adrenorecepetor agonists, corticosteroids

67
Q

How does an allergic reaction work?

A

Allergen activates CD4 cells –> Th2 –> IL-4,5,13 release –> B cell differentiation into plasma cells that produce IgE

68
Q

What is the most common autoimmune disease?

A

Graves’ thyroiditis

69
Q

What are examples of organ specific and non-organ specific autoimmune disease?

A

Organ-specific: Type I diabetes, graves’ thyroiditis

Non-organ specific: systemic lupus erythematosus, rheumatoid arthritis

70
Q

What are serum autoantibodies?

A

Example of breakage of self tolerance; usually IgG class

71
Q

What is myasthenia gravis?

A

Autoimmune disease: antibody to the ACh receptor –> muscular weakness and fatigue

72
Q

How is diabetes T cell mediated?

A
  1. CD8 T cells kill beta cells
  2. CD4 T cells mediate inflammation
  3. Failure of Treg to suppress
73
Q

What are the differences between primary and secondary immunodeficiencies?

A

Primary: inherited defect, rare
Secondary: acquired defect, common

74
Q

What is Di George syndrome?

A

No T cells –> often abnormalities of heart and facial features

75
Q

What is SCID?

A

Severe combined immune deficiency: no B and T cells

76
Q

What is chronic granulomatous disease?

A

Neutrophils can’t kill bacteria

77
Q

What is hypergammaglobulinemia?

A

Absence of CD40 ligand on T cells (important for communication with B cells) –> you can only make IgM

78
Q

What is HAART?

A

Highly active antiretroviral therapy; used for AIDS against HIV

79
Q

What are examples of iatrogenic immune deficiency?

A

Anti-TNFalpha for rheumatoid arthritis –> mycobacterial infections
Anti-IL17 for psoriasis –> fungal infections

80
Q

How do cancers hide from immune attack?

A

Cancer cell: expresses PD-L1 which interacts with programmed death (PD) receptors on effector cells –> stops killing of cancer cell

81
Q

How are organisms that cause infectious diseases grouped?

A 
Parasites: helminths and protozoa
Fungi
Bacteria
Viruses
Prions
82
Q

Which organisms are microparasites and which are macro?

A

Macro: helminths
Micro: protozoa, bacteria, fungi, viruses

83
Q

What are the most serious helminth infections?

A

Multicellular

Tapeworms (taenia solium) and flukes (schistosoma mansoni)

84
Q

What are characteristics of protozoa and what are some examples?

A

Single cell organisms; active growth stage (trophozoite) and dormant stage (cyst); malaria, toxoplasmosis, leishmaniasis

85
Q

What are characteristics of fungi?

A

Grow as single cell (yeast), branched filaments (hyphae –> form mycelium) or both (dimorphic fungi); thick cell wall composed of chitin

86
Q

What is peptidoglycan?

A

Also known as mucopeptide or murein; polymer of hexose sugars NAG and NAM and aa (tetrapeptide chain)

87
Q

Which bacteria cannot be seen with Gram stain?

A

Acid fast bacteria (outer membrane of free mycolic acids and polypeptides); mycobacterium tubercolosis

88
Q

What is the structure of capsules?

A

Gelatinous layer outside cell wall, primarily composed of polysaccharides; antiphagocytic

89
Q

What are the functions of pili?

A

Attachment and conjugation

90
Q

What are spores?

A

Only produces by some gram+ bacteria (bacillus and clostridium species); keratin-like coat confers resistance to heat, chemicals and drying

91
Q

What is the structure of viruses?

A

DNA or RNA; capsid core; polymerase protein; envelope (sometimes)

92
Q

What are capsids?

A

Constructed from small number of virally-encoded protein subunits (capsomeres)
3 types of symmetry: icosahedral, helical, complex

93
Q

Which viruses have a complex capsid?

A

Poxviruses

94
Q

What are the differences between resident and transient flora?

A

Resident: re-establishes itself, not removed by routine hand wash, not associated with transmission of infection, most common is Staph. epidermidis
Transient: doesn’t re-establish itself, removed by routine hand wash, associated with transmission of infection, most common is Staph. aureus

95
Q

What are opportunistic infections?

A

Caused by non-pathogenic microorganisms that act as pathogens in certain circumstances

96
Q

What is immunopathogenesis?

A

Primary cause of cell death in many infections, caused by killing of infected cells by the host immune system

97
Q

What is the difference between symptom, sign and syndrome?

A

Symptom: subjective features of disease experienced only by the patient
Sign: objective manifestations of disease that can be observed and measure by others
Syndrome: group of symptoms and signs of a disease

98
Q

What are the obligatory steps for infectious organisms?

A
  1. Entry and spread
  2. Evasion
  3. Multiplication
  4. Transmission
99
Q

What are the stages of infectious disease progression?

A
  1. Incubation
  2. Prodrome
  3. Illness
  4. Recovery/convalescence
100
Q

What is the difference between sporadic, endemic, epidemic, pandemic?

A

Sporadic: occasional
Endemic: continuously present in the population
Epidemic: increase in numbers in an area in a short period of time
Pandemic: epidemic disease that has world-wide distribution

101
Q

What is the difference between superficial and systemic infection?

A

Superficial: self limiting, replication in epithelium at site of entry and damage is local
Systemic: replication at multiple sites due to infection of deeper tissues, spread through lymph and blood

102
Q

What are nosocomial infections?

A

any infection acquired in a hospital or medical facility. Can affect patients and health care workers and are common because: easily moved around by staff, patients or visitors, not always can be prevented by proper hand washing. Most common in hospitals: Staph. aureus, c-difficile…

103
Q

What are some examples of antibiotic-resistant bacteria?

A

Methicillin resistant S. aureus (MRSA), VRE and CPE

104
Q

Which are the determinants of pathogenesis?

A

Opportunism, attachment, invasiveness, virulence, cellular pathogenesis

105
Q

What does tissue tropism mean?

A

Different tissues within the host that are infected by the pathogen

106
Q

What is a permissive cell?

A

One that allows the pathogen to replicate

107
Q

How do bacteria spread to deeper tissues?

A

Produce specific enzymes (invasins):

  1. Collagenase and hyaluronidase
  2. Coagulase: fibrin clot around bacteria to protect from phagocytosis
  3. Leukocidins
  4. Hemolysins
108
Q

What is virulence?

A

Degree of pathogenicity of a microorganism

Pathogenicity: ability of a microbe to cause disease

109
Q

How is virulence measured?

A

LD50 and ID50

110
Q

What are the differences between endo and exotoxins?

A

Endotoxins: from gram negative bacteria, LPS, genes contained in bacterial chromosome, low toxicity
Exotoxins: gram+ and - bacteria, secreted, genes in plasmid or phage, high toxicity, high antigenicity

111
Q

What are superantigens?

A

Toxins that stimulate the immune system; can bind to MHC II molecules non-specifically and stimulate a large number of T cells

112
Q

What is epidemiology?

A

Science that studies where and when diseases occur and how they are transmitted in a population

113
Q

What factors affect the spread of infection?

A

Reservoirs and modes of transmission

114
Q

What are emerging diseases?

A

Unrecognised disease, or previously recognised infection that has expanded into a new ecological niche, often accompanied by a significant change in pathogenicity

115
Q

What are zoonotic diseases?

A

Spread between animals and people

116
Q

What are the types of vehicle transmission?

A

Waterborne, airborne, foodborne

117
Q

What are the types of vector transmission?

A

Mechanical and biological

118
Q

What is the difference between vertical and horizontal transmission?

A

Vertical: between mother and child
Horizontal: person-to-person that is not mother to offspring

119
Q

What are the two main laboratory methods to confirm infection?

A

Direct detection: culture, microscopy and molecular methods

Indirect detection: presence of antibodies against the pathogen

120
Q

What are the two methods of detection of nucleic acids?

A

Hybridisation techniques with nucleic acid probes; PCR

121
Q

What is meant by titre?

A

Refers to antibody concentration in a sample and is associated with the number of times you can dilute a sample and still detect antibodies; retrospective

122
Q

Is it easier for RNA or DNA viruses to develop resistance?

A

RNA viruses: presence of error-prone polymerase enzyme

FBS2 (3 decks)

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